Scientists from the Tokyo University of Science discover for the first time the potential use of oxytocin as a therapeutic treatment for cognitive disorders such as Alzheimer’s Disease.
Cognitive disorders or neurodegenerative diseases such as Alzheimer’s Disease are sometimes caused by progressive degeneration of the neurons in the brain. This could result in other conditions such as dementia, intellectual deficiencies, as well as deterioration of motor and communication skills.
The accumulation of misfolded proteins, amyloid β (Aβ), is a main cause of Alzheimer’s Disease. These clusters of protein form around the neurons in the brain can disrupt its normal activity; triggering degeneration. Studies have found that aggregation of misfolded proteins in the hippocampus of the brain – the main learning and memory centre — can severely affect signal transmission of the neurons. Synaptic plasticity of the neurons could be lost, this function is crucial in the development of learning and cognitive functions in the hippocampus.
A team of scientists from the Tokyo University of Science, led by Professor Akiyoshi Saitoh has explored the potential of oxytocin — a hormone conventionally known for its role in the female reproductive system and in inducing the feelings of love and well-being – as a treatment for cognitive disorders.
“Oxytocin was recently found to be involved in regulating learning and memory performance, but so far, no previous study deals with the effect of oxytocin on misfolded protein-induced cognitive impairment,” Prof Saitoh says. Realizing this, Prof Saitoh’s group set out to connect the dots. Their findings are published in Biochemical and Biophysical Research Communication.
Using a mouse hippocampus model with Aβ, the team was able to confirm that perfusion of oxytocin showed increased signalling abilities, demonstrating that the hormone is able to reverse impairment of synaptic plasticity caused by Aβ.
The scientist went on further to blocking oxytocin receptors to observe whether oxytocin could reverse Aβ-induced impairment of synaptic plasticity without binding to these receptors. As expected, there was no reversal of the effect of Aβ when the receptors were blocked.
Blockage of certain chemical activities important in strengthening neuronal signalling potential and formation of memories, such as influx of calcium ions, showed that oxytocin could not reverse the synaptic plasticity damage caused by Aβ. Additionally, the team found that oxytocin itself does not have any effect on synaptic plasticity in the hippocampus, but it is somehow able to reverse the ill-effects of Aβ.
Professor Saitoh remarks, “This is the first study in the world that has shown that oxytocin can reverse Aβ-induced impairments in the mouse hippocampus.” This is only a first step and further research remains to be conducted in animal models and then humans before sufficient knowledge can be gathered to reposition oxytocin into a drug for Alzheimer Disease.
“At present, there are no sufficiently satisfactory drugs to treat dementia, and new therapies with novel mechanisms of action are desired. Our study puts forth the interesting possibility that oxytocin could be a novel therapeutic modality for the treatment of memory loss associated with cognitive disorders such as Alzheimer’s disease. We expect that our findings will open up a new pathway to the creation of new drugs for the treatment of dementia caused by Alzheimer’s disease.” Concludes Professor Saitoh. [APBN]